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TRANSCRIPT
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The yellow text is for extra
information – no need to copy
down
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First Line of DefenseFirst Line of Defense
Skin & mucous membranesPhysical barrierChemical barrier
○Lower pH○ “Flushing” of invades (tears, sweat,
mucus)○Antimicrobial proteins (lysozymes)
Digest cell walls
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Second Line of Second Line of DefenseDefense Non-specific Phagocytic leukocytes (WBC)
Neutrophils (60-70%)○Attracted to chemical signals from
damaged cells (chemotaxis)○Engulf & destroy microbes
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Second Line of Second Line of DefenseDefense
Monocytes (5%)○Develop into
long-lasting microphagesAttach to polysaccharides on
microbe’s surface○Some migrate, some are permanent
in lungs, liver, kidneys, brain, connective tissues, lymph nodes, & spleen
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Second Line of Second Line of DefenseDefense
Eosinophils (1.5%)○Defend against larger parasitic
invadersNatural killer cells (NK)
○Destroy virus-infected body cells
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Second Line of Second Line of DefenseDefense The Inflammatory Response
Precapillary arterioles dilatePostcapillary venules constrict
○ Inc. blood supply (redness & heat)○Pushes fluid out (edema)
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Second Line of Second Line of DefenseDefense
Initiated by chemical signals○Histamine
Produced by basophils (type of WBC) and mast cells in connective tissue
Increase dilation
○ProstaglandinsPromote blood flow to injury siteBoth inc. addition of clotting factors to the
area for healing
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Second Line of Second Line of DefenseDefense
Phagocytic cells attracted to area by chemokines (secreted by blood vessel endothelial cells & monocytes)
Pyrogens○Released by leukocytes○Raise body temp○ Inhibit growth & facilitate
phagocytosis
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Third Line of DefenseThird Line of Defense Specific Immunity
Lymphocytes○B cells & T cells○ In spleen, lymph nodes, & lymphatic
tissues○Detect specific antigens
Foreign molecules that elicit specific response
○Activate & produce certain antibodies○Have membrane antigen receptors
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Third Line of DefenseThird Line of Defense
○During early development, B cell or T cell develops receptors for any type of antigen (before contact)
○When contact with antigen, lymphocyte divides, differentiates, forming two clonesEffector cells (B cells secrete
antibody)Memory cells (long-living; have
receptors for antigen)
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Third Line of DefenseThird Line of Defense First contact – primary immune
response Second contact – secondary I.R.
Quicker (due to memory)Larger
scale
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Lymphocyte Lymphocyte DevelopmentDevelopment
From pluripotent stem cellsFetal bone marrow & liverIf then move to thymus T cell
If stays in bone marrow B cell
Key: self vs non-selfIf not, apoptosis
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Major Major Histocompatibility Histocompatibility
Complex (MHC)Complex (MHC) Cell surface glycoproteins Mark body cells as “self” Class I: on all nucleated cells Class II: specialized (macrophages &
B cells) Known as Antigen Presenting
Complex (APC)
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Major Major Histocompatibility Histocompatibility
Complex (MHC)Complex (MHC) Very polymorphicMakes almost all people unique
When infection, MHC presents antigen to T cell to alert them (antigen presentation)
Class I present to cytotoxic T cells (TC)
Class II present to helper T cells (TH)
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Immune ResponseImmune Response
Humoral ImmunityB cell activationDefend free invaders in body fluid
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Immune ResponseImmune Response Cell-mediated immunity
T cell activationWhen cytotoxic T cell activated by
Class I MHC, becomes active killer○Kills target cell with perforin
Protein that forms pores in target cell membrane
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Antibody-Mediated Antibody-Mediated DisposalDisposal 1) Neutralization
Antibody binds to & blocks antigen activity
2) OpsonizationBound antibodies enhance
macrophage attachment to the microbes
3) AgglutinationClumping of microbes
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Antibody-Mediated Antibody-Mediated DisposalDisposal
4) PrecipitationCross-linking of soluble antigens to
form immobile precipitate 5) Complement fixation
Activation of complement system○20 proteins inactive when no
infection○When infected, cascade of
activation starts○End result – lysis
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Plant Immune Plant Immune SystemSystem Plant defenses include molecular
recognition systems with systemic responses
Infection triggers chemical responsesDestroy infected and
adjacent cells, thus localizing the effects.
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Immunity Immunity ApplicationsApplications Active immunity
Achieved by exposure & recovery or vaccination
Passive immunityReceiving antibodies
Blood CompatibilityBased on surface antigen of RBC
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Immunity Immunity ApplicationsApplications Rh factor
RBC antigen (IgG)Mom Rh-, fetus Rh+
○Mother may have a T-dependent humoral responseAffects subsequent pregnancies
-Memory cells produce IgG
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Immunity Immunity ApplicationsApplications Tissues & Organs
MHC can cause rejection Allergies
Exaggerated responses to envi. antigens
Tend to involve IgE & mast cellsRelease of histamineCan result in abrupt dilation of blood
vessls, lowering bp (anaphylactic shock)
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Immunity Immunity ApplicationsApplications Autoimmune Diseases
Turns against itselfLupus, MS, diabetes, rheumatoid
arthritis
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Immunity Immunity ApplicationsApplications SCID
Both humoral & cell-mediated problems
Hodgkin’s disease○Damages lymphatic system
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Immunity Immunity ApplicationsApplications AIDS
Caused by HIVHIV-1 (more virulent strain) & HIV-2Both infect cells that have surface
CD4 moleculesCan also infect helper T cells,
B lymphocytes, & brain cells
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Immunity Immunity ApplicationsApplications
Entry of virus requires CD4 & a coreceptor protein○Fusin (CXCR4), found on helper T
cells○CCR5, found on macrophages
Integrates into genomeBody makes HIV antibodies intially
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Immunity Immunity ApplicationsApplications
Over time, viral load increasesHelper T cells become infected &
dieUse DNA-synthesis inhibitors,
reverse transcriptase inhibitors, & protease inhibitors to combat
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